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AX has been shown to buffer mitochondrial overload, which can be induced by physical exercise, as exercise inherently promotes ROS formation and mobilizes fuels within the mitochondria, but also by an HFD, as observed in obesity, which continuously stimulates the mitochondrial network in ATP production, fatty acid synthesis, and the consequent generation of ROS (Figure 2) [4,46]

(2020) demonstrated that GHK-Cu protected against bleomycin-induced pulmonary fibrosis in mice via anti-inflammatory mechanisms, reducing fibrotic tissue accumulation and preserving lung function